Saturday, June 17, 2017

There is sinus tachycardia. The T-waves are slightly peaked, suggesting hyperkalemia. But what is atypical is that the T-wave in V3 towers over the R-wave. And there is terminal QRS distortion in lead V3 (meaning there is neither a J-wave nor an S-wave).
The QTc is 462 ms. Terminal QRS distortion is never seen in normal variant ST Elevation in anterior leads (so-called early repolarization)These are suspicious for hyperacute T-waves and
anterior injury. The formula score is 24.8 (>23.4), also consistent
with anterior injury (STE60V3 = 2, QTcB = 460, RAV4 = 14.5), but terminal QRS distortion alone makes normal variant STE almost impossible and makes use of the formula particularly subject to false negatives.The above is what I thought when I saw this, so I went to the chart and found this history:A
type I diabetic aged approximately 35 years old presented with chest
pain, nausea, vomiting and diffuse abdominal pain. The patient was in
DKA with an anion gap of 35, a glucose of 1128, and a K of 5.5 mEq/L. pH = 7.17, pCO2 = 24, HCO3 = 8. Her T-waves were attributed to hyperkalemia, without further investigation.The patient was treated for DKA and admitted.One would not expect such profound T-wave changes from a K of only 5.5.

The patient did have a serial troponins (they are automatically ordered on critically ill patients) and they rose to a peak of 12.4 ng/ml, which is too high for a typical critical illness without MI. Here is her ECG the next day (with a normal K):

T-waves
are much more normal, less peaked, but also with better R-wave
amplitude. The ST segment is back to 0. Equation value is 23.0. There
is an S-wave in V3 now, although small.

Because
of the high troponin, echocardiography was done and showed a wall
motion abnormality in the anterior, anterolateral, and apical walls,
consistent with LAD myocardial infarction. Therefore, she underwent
angiography and had a 95% LAD thrombotic culprit that, fortunately,
had reperfused on its own (that's why the troponin was only 12). It was
stented. Had it not opened on its own, it could have resulted in a very large anterior wall MI.

The
possibility of anterior STEMI was not noticed during patient care. I
noticed it much later on looking through a random stack of EKGs. I mention this only to point out that these findings can be noticed, and differentiated from more benign etiologies, prospectively. This is NOT a retrospective finding.

Learning point: Hyperacute
T-waves and hyperkalemia may be confused, and they may be
simultaneous. Here the potassium was barely high enough to result in a
change in T-waves, so one should be especially suspicious in this case.

Superb case. The diffuse nature of these tall and peaked T waves (with narrow base) are clearly suggestive of hyperkalemia. But chest pain in the history — the terminal QRS distortion in lead V3 — and the no-more-than-modestly elevated serum K+ value of 5.5 mEq/L all provided clues to something in addition to hyperkalemia that could have been all-too-easy to overlook. Highly insightful and wonderful pick-up by Dr. Smith. THANKS for presenting!

I was looking at a stack of ECGs when I made the diagnosis. I did not know anything about the patient, including not knowing the troponin. It is the terminal QRS distortion that clued me in to LAD occlusion.

Is the terminal QRS distortion a consistent finding with hyperacute T waves? In that it would be a reliable sign to look for on a regular basis when attempting to deferentiate between the hyperacute T wave and peaked T from hyper K?

Disclaimer

Cases come from all over the world. Patient identifiers have been redacted or patient consent has been obtained. The contents of this site have not been reviewed nor approved by Hennepin County Medical Center and any views or opinions expressed herein do not necessarily reflect the views or opinions of Hennepin County Medical Center.

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